Gene linked to Tourette's syndrome
DNA defect may cause involuntary physical and verbal tics.
23 June 2003
JOHN WHITFIELD
Researchers have found a gene mutation that seems to lead to the
mental disorder Tourette's syndrome. The gene is normally switched
on in nerve cells; its disruption might make them hyperactive.
The gene has been detected in only one family so far. Studies of
more people with Tourette's syndrome are needed to confirm its
involvement in the condition.
"This gene might be involved in some people with Tourette's
syndrome, but it won't be in all of them," says the leader of the
team that found it, Ben Oostra, of Erasmus University, Rotterdam,
the Netherlands.
Tourette's syndrome affects about 1 in every 2,000 people. Sufferers
have involuntary physical and verbal tics that can include outbursts
of swearing. They often also have obsessive-compulsive disorder,
engaging in repetitive, ritualized behaviour.
In 1885, Gilles de la Tourette noticed that the condition now
bearing his name runs in families. Now genetic make-up is thought to
be a risk factor that combines with the environment to produce the
disorder.
Oostra's team studied a Californian family. The father has obsessive-
compulsive disorder, two of his children have this, plus tics and
other mental and physical problems. Tourette's syndrome is an
extreme version of obsessive-compulsive disorder, Oostra believes.
In all three people, a chunk of chromosome 2 is transplanted into
chromosome 7, the researchers found. This insertion breaks up a gene
on chromosome 7, called CNTNAP2, which helps to control the firing
of nerve cells.
"Some features of this gene are quite exciting," says child
psychiatrist James Leckman of Yale University, New Haven,
Connecticut. Other experiments have hinted that nerve cells in the
brains of those sufferering from Tourette's fire too easily. "This
suggests a mechanism by which the transmission of messages between
nerve cells might be juiced up," says Leckman.
Others doubt that this genetic abnormality has anything to do with
Tourette's syndrome. The number of people studied is too small to
draw strong conclusions, warns psychiatrist David Curtis of the
Royal London Hospital, UK.
Also, CNTNAP2 is not in a region of the genome previously suspected
of harbouring genes linked to Tourette's. "It might turn out to be
something, but it's a bit of a long shot," he says.
The children also have three copies of a small section of chromosome
2. It's this, rather than the single damaged gene, that probably
causes their more general mental and physical problems, says Oostra.
The team is testing other Tourette's sufferers to see whether they
have the same genetic change, and are studying the behaviour of a
mouse that lacks the gene. The gene does not point to any obvious
treatments, says Oostra.
References
Verkerk, A. et al. CNTNAP2 is disrupted in a family with Gilles de
la Tourette syndrome and obsessive compulsive disorder. Genomics,
82, 1 - 9, (2003). |Article|
© Nature News Service / Macmillan Magazines Ltd 2003
http://www.nature.com/nsu/030616/030616-23.html

Family's Genetic Abnormality Linked to Tourette's Syndrome
http://www.betterhumans.com/News/news.aspx?articleID=2003-06-25-2
Gabe Romain
Betterhumans Staff
Wednesday, June 25, 2003, 11:53:43 AM CT



A family with obsessive-compulsive disorder has led researchers to a
gene that may be involved in Tourette's syndrome.
The finding, by researchers from
http://web.eur.nl/english/
Erasmus University in Rotterdam, Netherlands, is reported in the
journalGenomics(readbstract)
Although they have only detected the gene in one family so far, the
researchers are hopeful that they're on to something.
"This gene might be involved in some people with Tourette's
syndrome, but it won't be in all of them," lead researcher Ben
Oostra told Nature News Service.
Tourette's syndrome
Tourette's syndrome is an inherited neurobehavioral disorder
characterized by sudden involuntary repetitive muscle movements and
vocalizations.
The disorder is named after Gilles de la Tourette, a neurologist who
described the syndrome in 1885.
Many people with Tourette's syndrome develop behavioral problems
such as obsessions and compulsions, inattention, hyperactivity and
impulsivity.
Symptom onset typically occurs during childhood or early
adolescence.
About one in every 2,000 people is affected.
Chromosomal abnormality
Oostra believes that Tourette's syndrome is an extreme version of
obsessive-compulsive disorder.
His team studied a California family in which the father and two
children suffer from OCD and the children additionally suffer from
tics and general mental and physical problems.
In all three family members, an abnormality involving chromosome 2
and chromosome 7 was found.
The abnormality is characterized by a portion of chromosome 2
interfering with a gene called CNTNAP2 that encodes for a membrane
protein that mediates cell-cell interactions in the nervous system.
CNTNAP2 resides on chromosome 7 and is involved in controlling the
firing of nerve cells.
Recent experiments show that nerve cells in the brain of people with
Tourette's syndrome fire too easily, suggesting the transmission of
messages between nerve cells might be working on overdrive.
The sample size for the current study relating a mutation in CNTNAP2
to such problems is small, however, and further studies are
necessary to validate the findings.
To this end, the researchers plan to continue tests on both people
with Tourette's syndrome and animal models.
Abstract
Cntnap2 is disrupted in a family with gilles de la tourette syndrome
and obsessive compulsive disorder
1 Annemieke J. M. H. Verkerka, Carol A. Mathewsb, Marijke Joossea,
Bert H. J. Eussena, Peter Heutinka, Ben A. Oostra , and the
Tourette Syndrome Association International Consortium for Geneticsa

a Department of Clinical Genetics, Erasmus MC, P.O. Box 1738, 3000
DR, Rotterdam, The Netherlands
b Neuropsychiatric Genetics Group, Department of Psychiatry,
University of California at San Diego, La Jolla, CA 92093-0810, USA

Received 19 September 2002; accepted 26 March 2003. ; Available
online 13 May 2003.

Abstract
Gilles de la Tourette syndrome (GTS) is a sporadic or inherited
complex neuropsychiatric disorder characterized by involuntary motor
and vocal tics. There is comorbidity with disorders like obsessive
compulsive disorder and attention deficit hyperactivity disorder.
Until now linkage analysis has pointed to a number of chromosomal
locations, but has failed to identify a clear candidate gene(s). We
have investigated a GTS family with a complex chromosomal
insertion/translocation involving chromosomes 2 and 7. The affected
father [46,XY,inv(2) (p23q22),ins(7;2) (q35–q36;p21p23)] and two
affected children [46,XX,der(7)ins(7;2)(q35–q36;p21p23) and 46,XY,der
(7)ins(7;2)(q35–q36;p213p23)] share a chromosome 2p21–p23 insertion
on chromosome 7q35–q36, thereby interrupting the contactin-
associated protein 2 gene (CNTNAP2). This gene encodes a membrane
protein located in a specific compartment at the nodes of Ranvier of
axons. We hypothesize that disruption or decreased expression of
CNTNAP2 could lead to a disturbed distribution of the K+ channels in
the nervous system, thereby influencing conduction and/or
repolarization of action potentials, causing unwanted actions or
movements in GTS.
Author Keywords: Gilles de la Tourette syndrome; Contactin-
associated protein; Potassium channel; Node of Ranvier;
Translocation
Corresponding author. Fax: +31 10 4089489.
complete list of members can be found under Acknowledgments in Am.
J. Hum. Genet. 65 (1999) 1428–1436.
Full article in PDF Must cut and past entire link below into your
browser. Unfortunately there is a fee to join the service and I can
not post the entire abstract here as I don't subscribe to the
service at the moment myself and don't have permissions. Sorry.
http://www.sciencedirect.com/science?_ob=MImg&_imagekey=B6WG1-
48KF9H9-2-B&_cdi=6809&_orig=search&_coverDate=07%2F31%
2F2003&_qd=1&_sk=999179998&view=c&wchp=dGLbVzb-
lSztA&_acct=C000050221&_version=1&_userid=10&md5=dcecf34026b258ead978
18b22b8d3921&ie=f.pdf
----------------------------------------------------------------


http://mp.medscape.com/cgi-bin1/DM/y/hcUj0GAQDt0Dyr0FcV50A8


Behavioral Therapy Helpful in Trichotillomania CME
News Author: Laurie Barclay, MD
CME Author: Bernard M. Sklar, MD, MS
Release Date: June 6, 2003; Valid for credit through June 6, 2004
Physicians - up to 0.25 AMA PRA category 1 credit(s)


June 6, 2003 — Behavioral therapy (BT) is more effective than
fluoxetine for the short-term treatment of trichotillomania,
according to the results of a randomized trial published in the May
issue of the Archives of General Psychiatry.
"Both [BT] and serotonin reuptake inhibitors have been reported
effective in the treatment of trichotillomania," write Agnes Van
Minnen, PhD, and colleagues from the University of Nijmegen in the
Netherlands. "Powerful randomized controlled studies comparing the
efficacy of BT and pharmacotherapy in the treatment of
trichotillomania are still lacking."
In this 12-week study, 43 patients with trichotillomania were
randomized to BT, treatment with 60 mg/d fluoxetine hydrochloride,
or a control group awaiting treatment. Of the 43 patients, 40
completed the trial, including 14 in the BT group, 11 in the
fluoxetine group, and 15 in the control group.
BT was superior to the other two groups in reducing the symptoms of
trichotillomania measured by effect sizes on the Massachusetts
General Hospital Hairpulling Scale (3.80 for BT; fluoxetine, 0.42;
and 1.09 for the control group). The percentage of patients who
experienced clinically significant improvements was 64% in the BT
group, 9% in the fluoxetine group, and 20% in the control group.
Patients in the BT group also fared better in terms of severity of
hair loss as rated by independent assessors. General
psychopathologic and depressive symptoms did not differ
significantly between groups.
Study limitations include self-reporting of severity of
trichotillomania symptoms, concerns regarding video ratings of hair
loss, a relatively small sample of self-referred patients, and
failure to address long-term outcomes.
"Behavioral therapy is highly effective for reducing symptoms of
trichotillomania in the short term, whereas fluoxetine is not," the
authors write. "Whether the superior treatment effects for BT will
be maintained in the long term is unknown. Follow-up studies are
essential to provide information about the stability of symptom
reduction."
Eli Lilly supported this study.
Arch Gen Psychiatry. 2003;60:517-522
Learning Objectives
Upon completion of this activity, participants will be able to:
Discuss the signs, symptoms, and treatment of trichotillomania.
Describe the results of a clinical trial comparing BT, fluoxetine,
and placement on a waiting list in the treatment of
trichotillomania.
Clinical Context
According to the Diagnostic and Statistical Manual of Mental
Disorders, Fourth Edition, trichotillomania is the recurrent pulling
out of one's hair resulting in noticeable hair loss. Sites of hair
pulling may include any region of the body in which hair may grow
(including axillary, pubic, and other regions), with the most common
sites being the scalp, eyebrows, and eyelids. Hair pulling may occur
in brief episodes scattered throughout the day or in less frequent
more sustained periods that can continue for hours.
Stressful circumstances frequently increase hair-pulling behavior,
but increased hair pulling also occurs in states of relaxation and
distraction (eg, when reading a book or watching television). An
increasing sense of tension is present immediately before pulling
out the hair. For some hair-pullers, tension does not necessarily
precede the act but is associated with attempts to resist the urge.
There is gratification, pleasure, or a sense of relief when pulling
out the hair.
Some individuals experience an "itchlike" sensation in the scalp
that is eased by the act of pulling hair. The diagnosis is not given
if the hair pulling is accounted for by another mental disorder (eg,
in response to a delusion or a hallucination) or is due to a general
medical condition (eg, inflammation of the skin or other
dermatologic condition). The disturbance causes significant
impairment in social, occupational, or other important areas of
functioning.
According to the authors of the current study, trichotillomania is
considered part of the spectrum of obsessive-compulsive disorders
because of its phenomenologic, epidemiologic, and neurobiologic
characteristics.
Several open-trial studies indicate that BT techniques are
successful in reducing or stopping hair pulling. Most of these
studies report the effectiveness of habit reversal, a BT program
that consists of self-monitoring, awareness training, training of an
incompatible response, preventive interruption of the habit,
overcorrection, and relaxation training.
In some studies, serotonergic medication was found to be effective
for trichotillomania. In several open-trial studies, clomipramine
and fluoxetine proved effective. Controlled studies, however,
yielded conflicting results. In one such study, clomipramine was
found to be more effective than desipramine. In another study, both
clomipramine and fluoxetine were shown to be more effective than
placebo treatment. However, two other controlled studies failed to
demonstrate a superior treatment effect for fluoxetine compared with
placebo treatment.
Thus far, only one randomized controlled study has compared BT with
psychopharmacological treatment. Ninan and colleagues, writing in
the January 2000 issue of the Journal of Clinical Psychiatry,
compared the treatment effects of cognitive BT, clomipramine
treatment (250 mg/d), and placebo in a sample of 16 patients with
trichotillomania. Cognitive BT proved more effective than
clomipramine, and clomipramine was found to be more effective than
placebo.
The present study compares BT with fluoxetine and placement on a
waiting list in the treatment of trichotillomania.
Study Highlights
Forty-three patients with trichotillomania entered a 12-week
randomized, waiting-list-controlled study of BT and fluoxetine (60
mg/d). Forty patients (14 in the BT group, 11 in the fluoxetine
group, and 15 in the waiting-list group) completed the trial.
Treatment effects were evaluated using the Massachusetts General
Hospital Hairpulling Scale, and severity of hair loss was rated by
independent assessors. In addition, general symptoms of
psychopathologic abnormalities and depression were measured.
Patients in the BT group showed a significantly greater reduction in
trichotillomania symptoms, higher effect sizes, and more clinically
significant changes than patients in the fluoxetine and waiting-list
groups. For severity of hair loss, a similar trend was also found in
favor of the BT group.
No significant differences between groups were established for
general psychopathologic and depressive symptoms.
Pearls for Practice
BT is highly effective for reducing symptoms of trichotillomania in
the short term, whereas fluoxetine is not.
Follow-up studies are essential to determine whether the superior
treatment effects for BT will be maintained in the long term.
Authors and Disclosures

This article may discuss investigational products or unapproved uses
of products regulated by the U.S. Food and Drug Administration.
News Author
Laurie Barclay, MD
Writer for Medscape Medical News
Disclosure: Dr. Barclay has reported no significant financial
interests.
CME Author
Bernard M. Sklar, MD, MS
Writer for Medscape Medical News
Disclosure: Dr. Sklar has disclosed that he has served as a
consultant for Schering-Plough.
News CME Staff
Deborah Flapan
Medscape Medical News Coordinator
Disclosure: Ms. Flapan has reported no significant financial
interests.
Elliott Silverman
News CME Manager
Disclosure: Mr. Silverman has reported no significant financial
interests.
Gary Vogin, MD
Clinical Reviewer and Senior Medical Editor, Medscape
Disclosure: Dr. Vogin has reported no significant financial
interests.
----------------------------------------------------------------



http://www.medscape.com/viewarticle/456666_3

Journal of Child Psychology and Psychiatry
May 2003 (Volume 44, Number 4)
The Psychosocial Functioning of Children and Spouses of Adults With
ADHD
Minde K, Eakin L, Hechtman L, et al.
Journal of Child Psychology and Psychiatry. 2003;44(4):637-646
The authors of this study sought to examine the psychosocial
functioning of families with attention-deficit/hyperactivity
disorder (ADHD) caretakers. They sought to (1) assess the prevalence
of ADHD in offspring of adults diagnosed with ADHD, (2) assess risk
for psychopathology and maladjustment in these offspring, (3) assess
the mental health and marital relationship of the spouse of the ADHD
adult parent.
Participants in the study included 33 adults with ADHD, 23 spouses,
and 63 children. The control group included 26 non-ADHD adults, 20
spouses, and 40 children. The adults with ADHD were selected from a
large study looking at the psychosocial functioning of 191 clinic-
referred adults with ADHD. Inclusion for the second study required
the presence of children between 4 and 17 years of age. The
comparison group was recruited through advertisements in the
community newspaper.
Results were as follows: 43% of children with ADHD parents met
criteria for ADHD vs 2% of comparison children. One family had 2
parents with ADHD and 3 offspring with ADHD. There was no
intergenerational continuity for subtype. ADHD mothers had more boys
with ADHD (4 of 11). ADHD fathers had more boys with ADHD (15 of
16). In terms of comorbidity, 70% of ADHD adults had other disorders
vs 15% of the comparison adults. Spouses of adults with ADHD had
more psychiatric disorders but not of a statistically significant
increase. Male spouses of ADHD women were more symptomatic than
comparison males with non-ADHD wives. Marital adjustment was much
poorer in families of ADHD adults, regardless of gender of the
parent; 58% of these parents reported maladjustment (vs 25% of
comparison group). However, spouses of the ADHD parent did not
always rate the marriage as poorly. Divorce rates were not
significantly different in the 2 groups. Assessment of the children
showed that those offspring diagnosed with ADHD had more anxiety and
oppositional defiant disorder than controls. The children with ADHD
also had poor psychosocial functioning, an effect not significantly
influenced by the presence of at least 1 healthy adult. However,
children without ADHD had improved functioning when at least 1
parent was healthy.
In their discussion, the authors noted that only 40% of ADHD adults
lived with a partner and only 31% had children. Average age was 32.5
years for ADHD males and 34.7 for ADHD females. Higher rates of
marriage and children had been expected. ADHD-related emotional
immaturity might have contributed to their delays in marriage and
entry into family life. It was hypothesized that children with an
ADHD parent would have more psychiatric disorders. The presence of
ADHD predicted comorbidity (73%) not presence of an ADHD parent. The
authors also had hypothesized that family and marital functioning
would be compromised by an adult with ADHD. It seemed that men
married to ADHD women were quite distressed and critical of their
wives but that women married to ADHD men were more supportive and
willing to compensate for the husband's impairments. Another
hypothesis was that parental psychopathology, marital discord, and
child psychopathology would be correlated. It seems that the
presence of ADHD in a child did not influence parental mental health
and that non-ADHD children seemed protected from impaired
functioning when at least 1 parent was mentally well. On the other
hand, almost half of the children with an ADHD parent had current
psychiatric disorder and 25% of spouses met criteria. These findings
underscore the importance of assessing family members when treating
an ADHD adult.


http://www.medscape.com/viewarticle/456666_2

Archives of General Psychiatry
May 2003 (Volume 60, Number 5)
Parent-Child Conflict and the Comorbidity Among Childhood
Externalizing Disorders
Burt SA, Krueger RF, McGue M, Iacono W
Archives of General Psychiatry. 2003;60(5):505-513
The authors of this study used data from the Minnesota Twin Family
Study (MTFS) to determine genetic and environmental factors
associated with the development of externalizing disorders in youth
exposed to parent-child conflicts. They entered parent-child
conflict, attention-deficit/hyperactivity disorder (ADHD),
oppositional defiant disorder (ODD), and conduct disorder (CD) into
a multivariate biometrics model to define the role of conflict as
part of a shared environmental factor common to ADHD, ODD, and CD.
Average age during the intake visit was 11 years. The cohort
included 753 same sex, reared-together monozygotic and dizygotic
twins (373 male pairs and 380 female pairs). The authors augmented
the sample with twins born between 1989 and 1991 to bring in 55
additional 11-year cohort pairs of twins. The total sample involved
1616 participants. They assessed parent-child relationships as well
as lifetime ADHD, ODD, and CD incidence.
Results were as follows. First, parent-child conflict appeared to
act as a common vulnerability that increased the risk for multiple
childhood disorders. The authors looked at other correlations
between psychosocial measures and ADHD, ODD, and CD in male and
female children. Conflict was the most highly correlated for all 3
externalizing disorders in both male and females. Low parental
involvement, low twin regard for parent, and low parent regard for
twin were separate variables associated with this factor. Second,
the genes common to ADHD, CD, and ODD may be the same genes that
influence conflict. The models showed that the genetic and nonshared
environmental disorder-specific paths were all significant. Third,
the shared environmental factor that influences conflicts accounted
for roughly a quarter of the shared environmental effects common to
ADHD, CD, and ODD. Although the study and its design have
limitations, the results have important implications. These results
include the probability that the source of psychiatric comorbidity
may lie in broad latent factors such as parent-child conflict and
family environment.

----------------------------------------------------------------


Prestwick Labs raises $15M round
Prestwick's lead drug, Xenazine, Used to Treat Tourette Syndrome
by Tyson Freeman
Prestwick Laboratories Inc., a biotechnology startup with an unusual
approach to drug discovery, announced Thursday, June 19, that it has
raised $15 million in a first-round financing.

The round was co-led by BioAsia Investments LLC of Palo Alto,
Calif., and Sofinnova Ventures of San Francisco, with investments
from Atlas Venture of Boston and BA Venture Partners of Foster City,
Calif.
Cooley Godward LLP represented Prestwick, while investor counsel was
Wilson Sonsini Goodrich & Rosati.
"Prestwick's late-stage product portfolio is one of the best we have
seen in a first-round venture financing," said Edgar Engleman,
general partner of BioAsia Investments. "Dr. [Kathleen] Clarence-
Smith clearly has demonstrated the ability to identify and bring in
promising therapeutic opportunities in the area."
"It is truly remarkable for a company at this stage to have a late-
stage development pipeline that will yield multiple approved drugs
within a reasonably short period of time," said Jim Healy, a general
partner at Sofinnova Ventures, in a statement.
Unlike many other biotechnology companies, Prestwick does no so-
called "basic research" of compounds. Instead of starting from
scratch to search for treatments, Prestwick searches for drugs
already under development at universities or at non-U.S.
pharmaceutical companies.
Prestwick finds opportunities in academia or from European companies
and takes the drugs through Phase II and Phase III trials in the
U.S., said Clarence-Smith, the company's founder, president and
chief scientific officer. "Our favorite opportunities are compounds
that have already been given to humans and have shown good results,"
she added.
That approach has been viewed with favor by investors searching for
a less risky, later-stage investment. "Investors always welcome risk
mitigated on someone else's money," said David Weaver, an analyst at
Bloomfield Hills, Mich.-based consulting firm Aimattech Consulting
LLC. He said that because Prestwick's lead drug has already been
accepted in the European market, it would be an easier sale to the
U.S. Food and Drug Administration (news - web sites) after clinical
trials in the U.S. "It cuts the timeframe and expense down," Weaver
said.
Weaver noted that with drugs already in use in Europe, Prestwick
could better predict the market potential for the U.S.
Prestwick's lead drug, Xenazine, has been shown effective in
multiple published clinical studies and has been approved for use in
Europe, Canada and Australia, but has not yet been approved in the
U.S., except under specific dispensing permits granted by the FDA.
The drug treats hyperkinetic movement disorders, such as
Huntington's disease, tardive dyskinesia and Tourette's syndrome.
Hyperkinesias, also known as chorea, are characterized by excessive,
involuntary purposeless and repetitive movements, which may involve
the face, limbs or the entire body.
While on the market as a schizophrenia treatment, it was given to
people with chorea and was effective. Clarence-Smith said that
nearly 100 million doses to 2,500 patients have been administered in
Europe with at least 80% of the patients showing improvement.
The drug has been registered in Europe with Cambridge Laboratories
of the U.K., said Clarence-Smith, but the company "saw going through
the FDA's process in the U.S. from Europe as a fairly daunting
prospect. So it sat on the shelf."
The market for the drug is not big enough for large pharmaceutical
companies, which puts its commercialization in a type of no-man's
land, said Frank Kung, managing partner at BioAsia Investments. "The
FDA approval process is expensive," he said, "so there is limited
incentive for large pharmaceuticals to undertake the effort and
smaller companies have not had the expertise or the willingness to
take it to the U.S."
The drug is distributed in limited doses by Dr. Joseph Jankovic of
Houston who has Investigation New Drug certification from the FDA.
Jankovic will be one of Prestwick's investigators in the clinical
trial planned to demonstrate the drug's performance.
Clarence-Smith said that the first patients will begin trials next
week and, eventually, the trial will encompass 16 locations in the
U.S. with between 70 and 90 patients.
Most of the proceeds will be used to finish Phase III studies of
Xenazine, and Clarence-Smith expects the drug to be on the market by
the third quarter of 2004.

Other drug candidates in Prestwick's portfolio include drugs for the
treatment of sleep apnea, Parkinson's, Alzheimer's and autism
----------------------------------------------------------------

Melbourne animator shows his feat of clay
June 15 2003

Harvie Krumpet follows the misfortunes of Harvie's life, dealing
with his case of Tourette's syndrome, the loss of a testicle and, of
course, love. The film was shot over 15 months between October 2001
and January 2003. Geoffrey Rush stars as the narrator.
Born in Melbourne, Elliot grew up on a prawn farm in South
Australia, as the son of an acrobatic clown and a tap-dancing mother.
As a child he was constantly creating things with egg cartons and
pipe cleaners, activity that his parents encouraged. "I was always
making things," he says.
He attended the VCA's film and television school, studying all forms
of filmmaking but when his hands touched a lump of plasticine,
Elliot was hooked.
A bookcase in his Windsor home is littered with statues of Harvey.
Tucked behind them are four AFI trophies, just a few of more than 50
awards he has won for his work.
Elliot says more films are in the pipeline and he's keen to get
stuck back into lumps of plasticine, creating more characters for
audiences to enjoy.
There's no tension on the set, Elliot insists, because his
stars, "are easy to work with and never talk back".
Harvie Krumpet will screen at the upcoming Melbourne International
Film Festival.


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